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cardioresp > Sem2 > Flashcards

Sem2 Flashcards

1
Q

APO signs/symptoms - history

A

SOB, orthopnoea/bendopnoea, paroxysmal nocturnal dyspnoea, cough, anxiety, (chest pain)

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2
Q

APO signs and symptoms - examination

A

Tachypnoea, course crackles, (wheeze), diaphoresis, tachycardia, hypertension, leg swelling/peripheral oedema

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3
Q

APO signs and symptoms - investigation

A

Decreased SpO2, chest x-ray/POCUS showing fluid, ECG

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4
Q

APO principles of treatment

A
  1. Symptomatic relief/reassurance
  2. Improve oxygenation
  3. Maintain cardiac output and perfusion of vital organs
  4. Reduce preload and after load
  5. Reduce excess extracellular fluid
  6. Identify and fix underlying cause
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5
Q

APO steps

A
  1. Inciting event e.g. AMI
  2. Decreased LV function
  3. Compensate by increasing stretch
  4. Pump failure so can’t overcome after load
  5. Back flow of blood into pulmonary circuit
  6. Increased hydrostatic pressure (more than oncotic) - lymphatic system can’t compensate
  7. Fluid in interstitial space increases membrane thickness - Fick’s law (sub clinical APO)
  8. Surfactant washed away
  9. Alveoli collapse decreasing surface area for gas exchange - Fick’s law
  10. Hypoxia/hypoxaemia causing SOB (clinical APO)
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6
Q

Shock definition

A

A state of cellular and tissue hypoxia due to reduced oxygen delivery and/or increased oxygen consumption and/or inadequate oxygen utilisation

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7
Q

Pre-shock/compensated shock characteristics

A

Compensatory mechanisms activated in response to diminished tissue perfusion: tachycardia, peripheral vasoconstriction, normal/mildly elevated blood pressure, mild/moderate hyperlactatemia

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8
Q

Shock characteristics

A

Compensatory mechanisms become overwhelmed: symptomatic tachycardia, dyspnoea, restlessness, diaphoresis, metabolic acidosis, hypotension, oliguria, cool/clammy skin

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9
Q

At what reduction in arterial blood volume do clinical signs and symptoms of shock begin showing (hypovolemic)?

A

20-25%

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10
Q

Progressive shock characteristics

A

Compensatory mechanisms completely overwhelmed, irreversible organ damage occurring. Signs and symptoms include: anuria, acute renal failure, acidemia, hypotension, hyperlatatemia, coma/death

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11
Q

4 causes of shock

A

Cardiogenic, obstructive, hypovolemic, distributive

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12
Q

Most common cause of shock

A

Septic

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13
Q

Types of hypotension for shock

A

Absolute (SBP <90, MAP <65), relative (drop in SBP >40), orthostatic (drop in SBP >20 or DBP >10 with standing), or profound (vasopressor-dependent)

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14
Q

Shock index

A

Shock index = heart rate/systolic blood pressure

SI>1 = bad

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15
Q

Pulse pressure in shock

A

Wide for distributive shock, narrow in other forms

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16
Q

Causes of oliguria in shock

A

Shunting of renal blood flow, kidney injury, intravascular volume depletion

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17
Q

Cellular effects of shock

A
  1. Cell membrane ion pump dysfunction
  2. Intracellular oedema
  3. Leakage of intracellular contents into extracellular space
  4. Inadequate regulation of intracellular pH
  5. Acidosis
  6. Endothelial dysfunction
  7. Further stimulation of inflammatory and anti inflammatory cascades
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18
Q

Endogenous causes of airway obstruction

A 
Airway oedema (anaphylaxis)
Mucus plug
Tongue displacement 
Infection (epiglottitis, croup)
Laryngospasm
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19
Q

Exogenous causes of airway obstruction

A

Foreign bodies

Trauma, burns, toxic gases

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20
Q

Foreign body airway obstruction epidemiology

A

80% of cases occur in children <3 years

Also common in elderly, people with dysphagia, altered conscious state, neurological problems (e.g. MND, Parkinson’s)

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21
Q

Is FBAO more common on left or right bronchus? Why?

A

Right (less steep angle)

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22
Q

Signs of effective coughing

A

Verbal response to questions, loud cough, able to breathe before coughing, fully responsive, stridor

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23
Q

Signs of ineffective coughing

A

Unable to vocalise, quite or silent cough, unable to breath, cyanosis, decreasing level of consciousness

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24
Q

Differential diagnosis for FBAO

A

Croup, epiglottitis, anaphylaxis/angioedema, laryngeal spasm

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25
Pneumothorax definition
Gas in the pleural space
26
Pneumothorax categorisation
Spontaneous vs traumatic Primary vs secondary (spontaneous) Iatrogenic vs non-iatrogenic (traumatic) Penetrating/open vs blunt/closed (non-iatrogenic)
27
Pneumothorax epidemiology
Men more than women | 1-37 per 100,000 per year
28
Pneumothorax signs and symptoms - history
Dyspnoea, sudden onset, pleuritic chest pain, (trauma), (ventilated pts)
29
Pneumothorax signs and symptoms - examination
Hypoxia, tachypnoea Tracheal deviation - late sign, subcutaneous emphysema/“bubble wrap” skin, hyper-resonant to percussion, unequal air entry - equal air entry not exclusion criteria, tachycardia, distended neck veins/ increased JVP - late sign, displaced apex beat - late sign, decreased conscious state - late sign, (Marfanoid syndrome)
30
Pneumothorax investigation
POCUS, decreasing EtCO2, hypotension not responding to fluids
31
Tension pneumothorax signs
Increased respiratory distress in awake pt Decreasing SpO2 to <92% despite O2 Decreasing conscious state Poor perfusion or increasing HR +/- decreasing BP Increasing peak inspiratory pressure (ventilator)/stiff bag Decreasing EtCO2 Increasing jugular venous pressure Tracheal shift
32
Mnemonic for TPT decompression
``` SMART Second intercostal space Mid-clavicular line Above rib below Right angle to chest Towards body of vertebrae ```
33
Vital signs for chest decompression (TPT)
GCS <10 | BP <70
34
What to do if pt is re-tensioning?
Flush cannula with 5-10mL of saline then (if ineffective) perform second decompression in close proximity on lateral side
35
SVT definition
Technically includes any tachdysrhymias arising from above the level of the Bundle of His/above ventricles Usually refers to AV nodal re-entry tachycardia (AVNRT) and sometimes AV re-entry tachycardia (AVRT)
36
Paroxysmal SVT (pSVT)
SVT with abrupt onset and offset
37
AVNRT characteristics and epidemiology
Most common cause of palpitations Typically paroxysmal Spontaneous or upon provocation (exertion, caffeine, alcohol, beta-agonists like salbutamol, sympathomimetics like amphetamines) More common in women May self resolve or continue indefinitely Rarely life threatening
38
AVNRT signs and symptoms
Presyncope or syncope (due to transient fall in blood pressure) Chest pain Dyspnoea Anxiety
39
AVNRT ECG features
P-waves absent or abnormal (retrograde p waves, p-wave inversion in leads II, III, aVF) Narrow QRS complex (unless co-existing bundle branch block, accessory pathway or rate-related aberrant conduction) Regular Rate 140-280bpm
40
AVRT characteristics
Anatomical re-entry due to accessory pathway bypassing AV node Wolf-Parkinsons-White and Lown-Ganong-Levine are two conditions that can cause this In WPW accessory pathway referred to as Bundle of Kent
41
AVRT ECG features
PR interval short <120ms (signal is not delayed by AV node) Delta wave QRS prolongation >120ms Rate >100
42
Signs of decompensating SVT
Wet chest (APO) Decreased perfusion/BP Decreased conscious state Ischaemic chest pain
43
Alpha pathway of AV node
Slow depolarisation | Fast repolarisation
44
Beta pathway of AV node
Fast depolarisation | Slow repolorisation
45
Where are the main baroreceptors located?
Carotid sinus and aortic arch
46
SVT signs and symptoms - history
Dyspnoea, choking sensation/abnormal sensation in throat, chest pain, palpitations, clammy/sweaty
47
SVT signs and symptoms - examination
Clear chest/normal airway appearance, cool, pale, clammy, grey skin
48
SVT signs and symptoms - investigation
ECG
49
When to do valsalva manoeuvre
Stable AVNRT or AVRT SBP >90 Standard valsava if manual handling or environmental concerns Repeat 2x at 2 min intervals (max 3 attempts)
50
4 phases of valsava
1. Onset of straining (increases BP) 2. Further increase in intrathoracic pressure (initially decreased BP then increases HR and BP) 3. Strain release (decreases intrathoracic pressure which decreases BP) 4. Increased BP activates baroreceptors leading to vagal tone outflow which decreases HR
51
How does adenosine work?
Binds to type 1 (A1) receptors and coupled to Gi-proteins Opens potassium channels (hyperpolarises cell) and inhibits calcium channels (prevents calcium entry into cell) This means cell can’t reach threshold potential so it can’t depolarise resulting in a short period of asystole before the SA node takes over
52
R-on-T phenomenon
Occurs when shock is delivered during relative refractory period (latter part of T-wave) which can induce VF
53
First degree AV block
Prolonged PR interval >0.20 sec (sometimes so prolonged it goes into T-wave) Usually caused by electrolyte imbalance Not usually of much clinical significance
54
2nd degree type 1 AV block (Wenckebach)
Progressive prolongation of PR interval culminating in non-conducting P-wave (group beating) Can be caused by inferior MI, drugs like beta-blockers, calcium channel blockers, amiodarone, digoxin, increased vagal tone (athletes), myocarditis, following cardiac surgery Usually benign and asymptomatic Low risk of progressing to third degree
55
Second degree type 2 (Hay)
Intermittent non-conducting p-waves without progressive prolongation of PR interval Can be caused by anterior MI, hyperkalaemia, cardiac surgery, inflammatory conditions, drugs like beta-blockers, calcium channel blockers, digoxin, amidodarone More likely to be associated with haemodynamic compromise, severe bradycardia and progression to 3rd degree
56
Third degree/complete heart block
Severe bradycardia due to absence of AV conduction AV dissociation - independent atrial and ventricular rates Causes are same as for second degree type 2 Pts at high risk for ventricular standstill and sudden cardiac death
57
Bradycardia categorisation
Regular or irregular | Narrow or wide complex
58
Mild bradycardia vs marked bradycardia
``` Mild = 50-60bpm Marked = 30-45bpm ```
59
Signs and symptoms of marked bradycardia
``` Decreased BP (80-90mmHg) Decreased perfusion Cool, pale, clammy skin Weak/absent pulse Agitated, confused, light headed, unconscious Chest pain Dyspnoea ```
60
Cardioprotective characteristic of bradycardia
Slower HR may be beneficial for ACS as it reduces workload/oxygen demand of the heart minimising extension of infarction and the potential to develop a life threatening rhythm
61
Signs of unstable bradycardia
Less than adequate perfusion (including acute STEMI and ischaemic chest pain) Profound bradycardia (<40bpm) and APO Runs of VT or ventricular escape rhythms HR <20bpm
62
Cardiomyopathy definition
Myocardial disorder in which the heart muscle is structurally and functionally abnormal in the absence of coronary artery disease, hypertension, valvular disease, and congenital heart disease sufficient to explain the observed myocardial abnormality
63
Bradycardia CPG care objectives
To increase HR where bradycardia is causing haemodynamic compromise, heart failure or life threatening arrhythmia
64
Pulmonary oedema CPG care objectives
Nitrates treat underlying cause of cardiogenic APO and should be administered to all patients presenting in symptomatic cardiogenic APO unless contraindicated CPAP is an appropriate treatment for respiratory failure associated with APO while the underlying cause is addressed. It may be required in patients unresponsive to nitrates or where respiratory failure is significant enough to require immediate treatment concurrent with nitrates Furosemide is not an appropriate first line treatment in hypertensive patients with a sympathetically driven APO. Nitrates and CPAP (where required) should be the initial priority. Where the patient is normotensive or hypertension has been corrected with nitrates, furosemide may be considered
65
Narrow complex tachycardia CPG care objectives
Rapid termination of life threatening arrhythmias and transport to a facility capable of definite care Rapid transport to facilitate the treatment of the arrhythmia where treatment is not available in the prehospital environment Early termination of stable SVT where possible, following ECG capture
66
Shock CPG care objectives
To achieve a perfusion target appropriate to the patient’s condition
67
Upper airway obstruction CPG care objectives
To identify and treat with the appropriate degree of urgency the potential airway obstruction indicated by stridor in adults

cardioresp (3 decks)

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